Moreover, two cell apoptosis modulators, Jun-B and lipocalin-2, are also recognized as interacting with the HGF/c-MET pathway.251 Another study demonstrated that the phosphorylation of RhoA, which is a biomarker highly mutated in diffuse GC patients, may be dependent on c-MET activity.252 Notably, a c-MET inhibitor prevented GC cell growth only in GC cells transfected with wild-type RhoA but not Y42 mutant RhoA in vivo and in vitro. The gene discussed is RHOA; the disease is gastric cancer.